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Kazuyuki Ikeda - One of the best experts on this subject based on the ideXlab platform.
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comparison of effects of sevoflurane nitrous oxide and Enflurane nitrous oxide on myocardial contractility in humans load independent and noninvasive assessment with transesophageal echocardiography
Anesthesiology, 1993Co-Authors: Mutsuhito Kikura, Kazuyuki IkedaAbstract:BACKGROUND: Few studies have been reported on the direct depressive effects of sevoflurane on myocardial contractility in humans. Direct assessment of contractile state is possible by examining the slope of left ventricular end-systolic wall stress (LVESWS) versus velocity of circumferential fiber shortening with heart rate corrected (Vcfc) relationship with echocardiography. Using this contractile index, the effects of sevoflurane/nitrous oxide were compared with that of Enflurane/nitrous oxide on myocardia contractility in humans. METHODS: Twenty-eight subjects were studied during either sevoflurane/nitrous oxide or Enflurane/nitrous oxide anesthesia. Systolic, diastolic, and mean arterial blood pressure, heart rate, and transesophageal echocardiographic data were determined at 0.9 MAC and 1.35 MAC of sevoflurane or Enflurane, both with 60% N2O, and at 1.6 MAC of sevoflurane with 60% N2O. Furthermore, another 28 awake subjects were studied with transthoracic echocardiography to examine the contractile state at awake state, and echocardiograms, heart rate, and arterial blood pressure were recorded. RESULTS: Heart rate did not changed significantly in either group. Enflurane/nitrous oxide produced significantly greater decrease in arterial blood pressure than did sevoflurane/nitrous oxide. The Vcfc at each anesthetic dose in both anesthetic groups was significantly less than that in the awake subjects group. Sevoflurane/nitrous oxide produced no significant change in Vcfc at 1.5 MAC, whereas Enflurane/nitrous oxide caused significant dose-related decrease in Vcfc. Vcfc produced by sevoflurane/nitrous oxide was significantly greater than that produced by Enflurane/nitrous oxide. There was no significant difference in LVESWS (index of afterload) between the groups. With respect to the LVESWS-Vcfc relationship, myocardial contractility was significantly depressed in both the sevoflurane and the Enflurane groups compared to the awake subjects group. However, myocardial contractility produced by Enflurane/nitrous oxide was significantly less than that by sevoflurane/nitrous oxide at equiMAC concentration. CONCLUSIONS: The results of the present study suggest that sevoflurane has fewer depressant effects on cardiac function than does Enflurane.
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uptake and biotransformation of sevof lurane in humans a comparative study of sevof lurane with halothane Enflurane and isoflurane
Journal of Clinical Anesthesia, 1990Co-Authors: Yoshito Shiraishi, Kazuyuki IkedaAbstract:Abstract Study Objective: To compare the volatile anesthetic sevoflurane with halothane, enfurane, and isof urane on the uptake and biotransformation in humans. Design: Prospective pharmacokinetic study of sevofurane administration in human subjects. Setting: Inpatient surgery clinic at a university medical center. Patients: Thirty-two Japanese patients, free of systemic diseases, undergoing minor elective surgery with endotracheal general anesthesia. Interventions: The patients were assigned randomly to one of four groups: halothane, Enflurane, isofurane, or sevofurane. One of the four volatile anesthetics being investigated [equivalent to 1.1 minimum alveolar concentration (MAC): halothane, 0.85%; enfurane, 1.85%; isofurane, 1.27%; and sevofurane, 1.88%; in inspired concentrations throughout the first hour of anesthesia] was administered for 60 minutes. Measurements and Main Results: In all patients, serum and urinary fluoride concentrations were measured. The concentrations of all gases were measured separately with a mass spectrometer. The cumulative uptake of each anesthetic agent during a certain period was calculated as an integration of the uptake rate per minute. The results for one-hour inhalation of sevofurane (1.1 MAC) showed an uptake (corrected for body surface area and MAC) of 490 ml/m 2 /MAC and estimated degradation rate of 3.3%. For purposes of comparison, similar studies of halothane (uptake, 653 ml/m 2 /MAC; degradation rate 15.7%), enfurane (1150 ml/m 2 /MAC; 1.3%), and isofurane (439 ml/m 2 /MAC; 0.6%) were also conducted. Sevofurane had a peak serum inorganic fluoride concentration of 19.3 μmol/L, and no abnormality in hepatic or renal functions was observed in any of the subjects during the two weeks postoperatively. Conclusions: Accurate determinations of uptake and degradation rate for sevoflurane and three other volatile anesthetics in Japanese patients were obtained. These findings have established that, despite its relatively large MAC *1.71%), sevoflurane has a small uptake due to its low solubility. However, the degradation rade was shown to be as high as 3.3%, resulting in a higher serum fluoride concentration than seen after administration of isoflurane, halothane, and (possibly) Enflurane.
Joan J Kendig - One of the best experts on this subject based on the ideXlab platform.
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Enflurane decreases glutamate neurotransmission to spinal cord motor neurons by both pre and postsynaptic actions
Anesthesia & Analgesia, 2003Co-Authors: Gong Cheng, Joan J KendigAbstract:UNLABELLED: We have previously reported volatile anesthetic actions on glycinergic inhibitory transmission to spinal motor neurons. The present study is a comparable set of experiments on glutamatergic excitatory transmission. We tested the hypothesis that the balance between excitation and inhibition is shifted toward inhibition by larger depressant actions on excitation. Patch-clamp techniques were used to study spontaneous and evoked glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid currents in rat spinal cord slices. Enflurane (0.6 mM, 1 minimum alveolar anesthetic concentration) significantly decreased spontaneous miniature current frequencies either when sodium channels were blocked (miniature excitatory postsynaptic currents, mEPSCs), or when sodium channels were not blocked (spontaneous excitatory postsynaptic currents, sEPSCs). Enflurane did not affect mEPSC or sEPSC amplitude or kinetics. The effects on mEPSCs and sEPSCs did not differ. Enflurane significantly decreased both amplitude and area of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-evoked currents with no change in kinetics (P < 0.05 and 0.01, respectively). In contrast, Enflurane increased miniature glycinergic current frequency when sodium channels were blocked, and prolonged glycinergic current duration. Enflurane actions on glutamatergic excitatory transmission are purely depressant both pre- and postsynaptically, whereas glycinergic inhibition is enhanced presynaptically under some conditions, and always prolonged postsynaptically. Thus, Enflurane shifts the balance between synaptic excitation and inhibition in the direction of inhibition. IMPLICATIONS: Explanations proposed for anesthetic-induced central nervous system depression include enhancement of synaptic inhibition and depression of excitation. The results reported herein suggest that, in the case of Enflurane, the mechanism is a shift in the balance toward inhibition. Excitation is uniformly depressed by multiple mechanisms, whereas some anesthetic actions tend to enhance inhibition.
D A Terrar - One of the best experts on this subject based on the ideXlab platform.
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effects of propofol and Enflurane on action potentials membrane currents and contraction of guinea pig isolated ventricular myocytes
British Journal of Pharmacology, 1992Co-Authors: R M Puttick, D A TerrarAbstract:1. The effects of two general anaesthetics, propofol and Enflurane, on electrical activity and contractions were investigated in single myocytes isolated from guinea-pig ventricles. 2. Propofol and Enflurane depressed the plateau and shortened the duration of action potentials. 3. Under voltage-clamp conditions, propofol and Enflurane reduced the amplitude of inward calcium current and of additional inward current activated by cytosolic calcium. 4. Contractions (measured with an optical technique) accompanying either action potentials or second inward currents (in response to depolarizations to 0 mV) were reduced by both anaesthetics. The mechanisms for calcium entry during contractions accompanying pulses to positive potentials such as +60 mV are thought to differ from those accompanying second inward currents which are evoked by pulses from -40 to 0 mV. Enflurane enhanced the amplitudes of contractions accompanying pulses to positive potentials; in contrast these contractions were depressed by propofol. 5. In experiments where recovery processes were investigated by use of pairs of voltage-clamp pulses with a variable interval between them, Enflurane but not propofol slowed the recovery of contractions and calcium-activated 'tail' currents. These observations are consistent with the hypothesis that Enflurane may impair calcium handling by the sarcoplasmic reticulum whereas propofol has little, if any, effect at this site. 6. In conclusion, the actions of propofol and Enflurane on second inward currents contribute to their effects on action potentials and contraction. The negative inotropic effect of both anaesthetics may result partly from reduced calcium influx to trigger contraction, and for Enflurane, partly from an impairment of calcium handling by the sarcoplasmic reticulum.
B Antkowiak - One of the best experts on this subject based on the ideXlab platform.
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effects of isoflurane and Enflurane on gabaa and glycine receptors contribute equally to depressant actions on spinal ventral horn neurones in rats
BJA: British Journal of Anaesthesia, 2006Co-Authors: Christian Grasshoff, B AntkowiakAbstract:Background Volatile anaesthetics are widely used agents in clinical anaesthesia, although their mechanism of action is poorly understood. In particular, the dominant molecular mechanisms by which volatile anaesthetics depress spinal neurones and thereby mediate spinal effects such as immobility have recently become a matter of dispute. As GABAA and glycine receptors are potential candidates we investigated the impact of both receptor systems in mediating the depressant effects of isoflurane and Enflurane on spinal neurones in rats. Methods The effects of isoflurane and Enflurane on spontaneous action potential firing were investigated by extracellular voltage recordings from ventral horn interneurones in cultured spinal cord tissue slices obtained from embryonic rats (E 14–15). Results Isoflurane and Enflurane reduced spontaneous action potential firing. Concentrations causing half-maximal effects (isoflurane: 0.17 mM; Enflurane: 0.50 mM) were less than EC50-immobility (isoflurane: 0.32 mM; Enflurane: 0.62 mM). Effects of isoflurane were mediated by 39% by glycine receptors and 36% by GABAA receptors. The effects of Enflurane were mediated 26% by GABAA receptors and 29% by glycine receptors. Conclusion These results demonstrate that the effects of isoflurane and Enflurane on GABAA and glycine receptors contribute almost equally to their depressant actions on spinal ventral horn neurones in rats. The fraction of inhibition mediated by both receptor systems differs between specific volatile anaesthetics. Our data argue against the theory that a dominant molecular mechanism accounts for spinal effects of volatile anaesthetics.
Gong Cheng - One of the best experts on this subject based on the ideXlab platform.
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Enflurane decreases glutamate neurotransmission to spinal cord motor neurons by both pre and postsynaptic actions
Anesthesia & Analgesia, 2003Co-Authors: Gong Cheng, Joan J KendigAbstract:UNLABELLED: We have previously reported volatile anesthetic actions on glycinergic inhibitory transmission to spinal motor neurons. The present study is a comparable set of experiments on glutamatergic excitatory transmission. We tested the hypothesis that the balance between excitation and inhibition is shifted toward inhibition by larger depressant actions on excitation. Patch-clamp techniques were used to study spontaneous and evoked glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid currents in rat spinal cord slices. Enflurane (0.6 mM, 1 minimum alveolar anesthetic concentration) significantly decreased spontaneous miniature current frequencies either when sodium channels were blocked (miniature excitatory postsynaptic currents, mEPSCs), or when sodium channels were not blocked (spontaneous excitatory postsynaptic currents, sEPSCs). Enflurane did not affect mEPSC or sEPSC amplitude or kinetics. The effects on mEPSCs and sEPSCs did not differ. Enflurane significantly decreased both amplitude and area of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-evoked currents with no change in kinetics (P < 0.05 and 0.01, respectively). In contrast, Enflurane increased miniature glycinergic current frequency when sodium channels were blocked, and prolonged glycinergic current duration. Enflurane actions on glutamatergic excitatory transmission are purely depressant both pre- and postsynaptically, whereas glycinergic inhibition is enhanced presynaptically under some conditions, and always prolonged postsynaptically. Thus, Enflurane shifts the balance between synaptic excitation and inhibition in the direction of inhibition. IMPLICATIONS: Explanations proposed for anesthetic-induced central nervous system depression include enhancement of synaptic inhibition and depression of excitation. The results reported herein suggest that, in the case of Enflurane, the mechanism is a shift in the balance toward inhibition. Excitation is uniformly depressed by multiple mechanisms, whereas some anesthetic actions tend to enhance inhibition.